Association between fine particulate matter (PM2.5) and infant mortality in a North Carolina birth cohort (2003-2015).

Background: While the association between fine particulate matter (PM2.5) and adult mortality is well established, few studies have examined the association between long-term PM2.5 exposure and infant mortality. Methods: We conducted an unmatched case-control study of 5992 infant mortality cases and 60,000 randomly selected controls from a North Carolina birth cohort (2003-2015). PM2.5 during critical exposure periods (trimesters, pregnancy, first month alive) was estimated using residential address and a national spatiotemporal model at census block centroid. We fit adjusted logistic regression models and calculated odds ratios (ORs) and 95% confidence intervals (CIs). Due to differences in PM2 .5 over time, we stratified analyses into two periods: 2003-2009 (mean = 12.1 µg/m3, interquartile range [IQR]: 10.8-13.5) and 2011-2015 (mean = 8.4 µg/m3, IQR: 7.7-9.0). We assessed effect measure modification by birthing parent race/ethnicity, full-term birth, and PM2.5 concentrations. Results: For births 2003-2015, the odds of infant mortality increased by 12% (95% CI: 1.06, 1.17) per 4.0 µg/m3 increase in PM2.5 exposure averaged over the pregnancy. After stratifying, we observed an increase of 4% (95% CI: 0.95, 1.14) for births in 2003-2009 and a decrease of 15% (95% CI: 0.72, 1.01) for births in 2011-2015. Among infants with higher PM2.5 exposure (≥12 µg/m3) during pregnancy, the odds of infant mortality increased (OR: 2.69; 95% CI: 2.17, 3.34) whereas the lower exposure (<8 µg/m3) group reported decreased odds (OR: 0.50; 95% CI: 0.28, 0.89). Conclusions: We observed differing associations of PM2.5 exposure with infant mortality across higher versus lower PM2.5 concentrations. Research findings suggest the importance of accounting for long-term trends of decreasing PM2.5 concentrations in future research.

Estimating ambient air pollutant concentrations outside and inside homes in the Subpopulations and Intermediate outcomes in COPD air pollution (SPIROMICS air) cohort.

BACKGROUND: Valid, high-resolution estimates of population-level exposure to air pollutants are necessary for accurate estimation of the association between air pollution and the occurrence or exacerbation of adverse health outcomes such as Chronic Obstructive Pulmonary Disease (COPD). OBJECTIVES: We produced fine-scale individual-level estimates of ambient concentrations of multiple air pollutants (fine particulate matter [PM2.5], NOX, NO2, and O3) at residences of participants in the Subpopulations and Intermediate Outcomes in COPD Air Pollution (SPIROMICS Air) study, located in seven regions in the US. For PM2.5, we additionally integrated modeled estimates of particulate infiltration based on home characteristics and measured total indoor concentrations to provide comprehensive estimates of exposure levels. METHODS: To estimate ambient concentrations, we used a hierarchical high-resolution spatiotemporal model that integrates hundreds of geographic covariates and pollutant measurements from regulatory and study-specific monitors, including ones located at participant residences. We modeled infiltration efficiency based on data on house characteristics, home heating and cooling practices, indoor smoke and combustion sources, meteorological factors, and paired indoor-outdoor pollutant measurements, among other indicators. RESULTS: Cross-validated prediction accuracy (R2) for models of ambient concentrations was above 0.80 for most regions and pollutants. Particulate matter infiltration efficiency varied by region, from 0.51 in Winston-Salem to 0.72 in Los Angeles, and ambient-source particles constituted a substantial fraction of total indoor PM2.5. CONCLUSION: Leveraging well-validated fine-scale approaches for estimating outdoor, ambient-source indoor, and total indoor pollutant concentrations, we can provide comprehensive estimates of short and long-term exposure levels for cohorts undergoing follow-up in multiple different regions.

Leveraging low-cost sensors to predict nitrogen dioxide for epidemiologic exposure assessment.

BACKGROUND: Statistical models of air pollution enable intra-urban characterization of pollutant concentrations, benefiting exposure assessment for environmental epidemiology. The new generation of low-cost sensors facilitate the deployment of dense monitoring networks and can potentially be used to improve intra-urban models of air pollution. OBJECTIVE: Develop and evaluate a spatiotemporal model for nitrogen dioxide (NO2) in the Puget Sound region of WA, USA for the Adult Changes in Thought Air Pollution (ACT-AP) study and assess the contribution of low-cost sensor data to the model's performance through cross-validation. METHODS: We developed a spatiotemporal NO2 model for the study region incorporating data from 11 agency locations, 364 supplementary monitoring locations, and 117 low-cost sensor (LCS) locations for the 1996-2020 time period. Model features included long-term time trends and dimension-reduced land use regression. We evaluated the contribution of LCS network data by comparing models fit with and without sensor data using cross-validated (CV) summary performance statistics. RESULTS: The best performing model had one time trend and geographic covariates summarized into three partial least squares components. The model, fit with LCS data, performed as well as other recent studies (agency cross-validation: CV- root mean square error (RMSE) = 2.5 ppb NO2; CV- coefficient of determination ( R 2 ) = 0.85). Predictions of NO2 concentrations developed with LCS were higher at residential locations compared to a model without LCS, especially in recent years. While LCS did not provide a strong performance gain at agency sites (CV-RMSE = 2.8 ppb NO2; CV- R 2 = 0.82 without LCS), at residential locations, the improvement was substantial, with RMSE = 3.8 ppb NO2 and R 2 = 0.08 (without LCS), compared to CV-RMSE = 2.8 ppb NO2 and CV- R 2 = 0.51 (with LCS). IMPACT: We developed a spatiotemporal model for nitrogen dioxide (NO2) pollution in Washington's Puget Sound region for epidemiologic exposure assessment for the Adult Changes in Thought Air Pollution study. We examined the impact of including low-cost sensor data in the NO2 model and found the additional spatial information the sensors provided predicted NO2 concentrations that were higher than without low-cost sensors, particularly in recent years. We did not observe a clear, substantial improvement in cross-validation performance over a similar model fit without low-cost sensor data; however, the prediction improvement with low-cost sensors at residential locations was substantial. The performance gains from low-cost sensors may have been attenuated due to spatial information provided by other supplementary monitoring data.

Air Pollution Exposure and Interstitial Lung Features in SPIROMICS Participants with Chronic Obstructive Pulmonary Disease.

Rationale: It is unknown whether air pollution is associated with radiographic features of interstitial lung disease in individuals with chronic obstructive pulmonary disease (COPD). Objectives: To determine whether air pollution increases the prevalence of interstitial lung abnormalities (ILA) or percent high-attenuation areas (HAA) on computed tomography (CT) in individuals with a heavy smoking history and COPD. Methods: We performed a cross-sectional study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), focused on current or former smokers with COPD. Ten-year exposure to particulate matter ⩽2.5 µm in aerodynamic diameter (PM2.5), nitrogen oxides (NOx), nitrogen dioxide (NO2), and ozone before enrollment CT (completed between 2010 and 2015) were estimated with validated spatiotemporal models at residential addresses. We applied adjusted multivariable modified Poisson regression and linear regression to investigate associations between pollution exposure and relative risk (RR) of ILA or increased percent HAA (between -600 and -250 Hounsfield units), respectively. We assessed for effect modification by MUC5B-promoter polymorphism (variant allele carriers GT or TT vs. GG at rs3705950), smoking status, sex, and percent emphysema. Results: Among 1,272 participants with COPD assessed for HAA, 424 were current smokers, and 249 were carriers of the variant MUC5B allele. A total of 519 participants were assessed for ILA. We found no association between pollution exposure and ILA or HAA. Associations between pollutant exposures and risk of ILA were modified by the presence of MUC5B polymorphism (P value interaction term for NOx = 0.04 and PM2.5 = 0.05) and smoking status (P value interaction term for NOx = 0.05; NO2 = 0.01; and ozone = 0.05). With higher exposure to NOx and PM2.5, MUC5B variant carriers had an increased risk of ILA (RR per 26 ppb NOx, 2.41; 95% confidence interval [CI], 0.97-6.0; and RR per 4 µg ⋅ m-3 PM2.5, 1.43; 95% CI, 0.93-2.2, respectively). With higher exposure to NO2, former smokers had an increased risk of ILA (RR per 10 ppb, 1.64; 95% CI, 1.0-2.7). Conclusions: Exposure to ambient air pollution was not associated with interstitial features on CT in this population of heavy smokers with COPD. MUC5B modified the association between pollution and ILA, suggesting that gene-environment interactions may influence prevalence of interstitial lung features in COPD.

Integrating traffic pollution dispersion into spatiotemporal NO2 prediction.

Accurately predicting ambient NO2 concentrations has great public health importance, as traffic-related air pollution is of major concern in urban areas. In this study, we present a novel approach incorporating traffic contribution to NO2 prediction in a fine-scale spatiotemporal model. We used nationally available traffic estimate dataset in a scalable dispersion model, Research LINE source dispersion model (RLINE). RLINE estimates then served as an additional input for a validated spatiotemporal pollution modeling approach. Our analysis uses measurement data collected by the Multi-Ethnic Study of Atherosclerosis and Air Pollution in the greater Los Angeles area between 2006 and 2009. We predicted road-type-specific annual average daily traffic (AADT) on road segments via national-level spatial regression models with nearest-neighbor Gaussian processes (spNNGP); the spNNGP models were trained based on over half a million point-level traffic volume measurements nationwide. AADT estimates on all highways were combined with meteorological data in RLINE models. We evaluated two strategies to integrate RLINE estimates into spatiotemporal NO2 models: 1) incorporating RLINE estimates as a space-only covariate and, 2) as a spatiotemporal covariate. The results showed that integrating the RLINE estimates as a space-only covariate improved overall cross-validation R2 from 0.83 to 0.84, and root mean squared error (RMSE) from 3.58 to 3.48 ppb. Incorporating the estimates as a spatiotemporal covariate resulted in similar model improvement. The improvement of our spatiotemporal model was more profound in roadside monitors alongside highways, with R2 increasing from 0.56 to 0.66 and RMSE decreasing from 3.52 to 3.11 ppb. The observed improvement indicates that the RLINE estimates enhanced the model's predictive capabilities for roadside NO2 concentration gradients even after considering a comprehensive list of geographic covariates including the distance to roads. Our proposed modeling framework can be generalized to improve high-resolution prediction of NO2 exposure - especially near major roads in the U.S.

Airway Tree Caliber and Susceptibility to Pollution-associated Emphysema: MESA Air and Lung Studies.

Rationale: Airway tree morphology varies in the general population and may modify the distribution and uptake of inhaled pollutants. Objectives: We hypothesized that smaller airway caliber would be associated with emphysema progression and would increase susceptibility to air pollutant-associated emphysema progression. Methods: MESA (Multi-Ethnic Study of Atherosclerosis) is a general population cohort of adults 45-84 years old from six U.S. communities. Airway tree caliber was quantified as the mean of airway lumen diameters measured from baseline cardiac computed tomography (CT) (2000-2002). Percentage emphysema, defined as percentage of lung pixels below -950 Hounsfield units, was assessed up to five times per participant via cardiac CT scan (2000-2007) and equivalent regions on lung CT scan (2010-2018). Long-term outdoor air pollutant concentrations (particulate matter with an aerodynamic diameter ⩽2.5 µm, oxides of nitrogen, and ozone) were estimated at the residential address with validated spatiotemporal models. Linear mixed models estimated the association between airway tree caliber and emphysema progression; modification of pollutant-associated emphysema progression was assessed using multiplicative interaction terms. Measurements and Main Results: Among 6,793 participants (mean ± SD age, 62 ± 10 yr), baseline airway tree caliber was 3.95 ± 1.1 mm and median (interquartile range) of percentage emphysema was 2.88 (1.21-5.68). In adjusted analyses, 10-year emphysema progression rate was 0.75 percentage points (95% confidence interval, 0.54-0.96%) higher in the smallest compared with largest airway tree caliber quartile. Airway tree caliber also modified air pollutant-associated emphysema progression. Conclusions: Smaller airway tree caliber was associated with accelerated emphysema progression and modified air pollutant-associated emphysema progression. A better understanding of the mechanisms of airway-alveolar homeostasis and air pollutant deposition is needed.

Evaluating low-cost monitoring designs for PM2.5 exposure assessment with a spatiotemporal modeling approach.

Determining the most feasible and cost-effective approaches to improving PM2.5 exposure assessment with low-cost monitors (LCMs) can considerably enhance the quality of its epidemiological inferences. We investigated features of fixed-site LCM designs that most impact PM2.5 exposure estimates to be used in long-term epidemiological inference for the Adult Changes in Thought Air Pollution (ACT-AP) study. We used ACT-AP collected and calibrated LCM PM2.5 measurements at the two-week level from April 2017 to September 2020 (N of monitors [measurements] = 82 [502]). We also acquired reference-grade PM2.5 measurements from January 2010 to September 2020 (N = 78 [6186]). We used a spatiotemporal modeling approach to predict PM2.5 exposures with either all LCM measurements or varying subsets with reduced temporal or spatial coverage. We evaluated the models based on a combination of cross-validation and external validation at locations of LCMs included in the models (N = 82), and also based on an independent external validation with a set of LCMs not used for the modeling (N = 30). We found that the model's performance declined substantially when LCM measurements were entirely excluded (spatiotemporal validation R2 [RMSE] = 0.69 [1.2 µg/m3]) compared to the model with all LCM measurements (0.84 [0.9 µg/m3]). Temporally, using the farthest apart measurements (i.e., the first and last) from each LCM resulted in the closest model's performance (0.79 [1.0 µg/m3]) to the model with all LCM data. The models with only the first or last measurement had decreased performance (0.77 [1.1 µg/m3]). Spatially, the model's performance decreased linearly to 0.74 (1.1 µg/m3) when only 10% of LCMs were included. Our analysis also showed that LCMs located in densely populated, road-proximate areas improved the model more than those placed in moderately populated, road-distant areas.

Indoor Pollution and Lung Function Decline in Current and Former Smokers: SPIROMICS AIR.

Rationale: Indoor pollutants have been associated with chronic obstructive pulmonary disease morbidity, but it is unclear whether they contribute to disease progression. Objectives: We aimed to determine whether indoor particulate matter (PM) and nitrogen dioxide (NO2) are associated with lung function decline among current and former smokers. Methods: Of the 2,382 subjects with a history of smoking in SPIROMICS AIR, 1,208 participants had complete information to estimate indoor PM and NO2, using individual-based prediction models, in relation to measured spirometry at two or more clinic visits. We used a three-way interaction model between time, pollutant, and smoking status and assessed the indoor pollutant-associated difference in FEV1 decline separately using a generalized linear mixed model. Measurements and Main Results: Participants had an average rate of FEV1 decline of 60.3 ml/yr for those currently smoking compared with 35.2 ml/yr for those who quit. The association of indoor PM with FEV1 decline differed by smoking status. Among former smokers, every 10 µg/m3 increase in estimated indoor PM was associated with an additional 10 ml/yr decline in FEV1 (P = 0.044). Among current smokers, FEV1 decline did not differ by indoor PM. The results of indoor NO2 suggest trends similar to those for PM ⩽2.5 µm in aerodynamic diameter. Conclusions: Former smokers with chronic obstructive pulmonary disease who live in homes with high estimated PM have accelerated lung function loss, and those in homes with low PM have lung function loss similar to normal aging. In-home PM exposure may contribute to variability in lung function decline in people who quit smoking and may be a modifiable exposure.

Exposure Disparities by Income, Race and Ethnicity, and Historic Redlining Grade in the Greater Seattle Area for Ultrafine Particles and Other Air Pollutants.

BACKGROUND: Growing evidence shows ultrafine particles (UFPs) are detrimental to cardiovascular, cerebrovascular, and respiratory health. Historically, racialized and low-income communities are exposed to higher concentrations of air pollution. OBJECTIVES: Our aim was to conduct a descriptive analysis of present-day air pollution exposure disparities in the greater Seattle, Washington, area by income, race, ethnicity, and historical redlining grade. We focused on UFPs (particle number count) and compared with black carbon, nitrogen dioxide, and fine particulate matter (PM2.5) levels. METHODS: We obtained race and ethnicity data from the 2010 U.S. Census, median household income data from the 2006-2010 American Community Survey, and Home Owners' Loan Corporation (HOLC) redlining data from the University of Richmond's Mapping Inequality. We predicted pollutant concentrations at block centroids from 2019 mobile monitoring data. The study region encompassed much of urban Seattle, with redlining analyses restricted to a smaller region. To analyze disparities, we calculated population-weighted mean exposures and regression analyses using a generalized estimating equation model to account for spatial correlation. RESULTS: Pollutant concentrations and disparities were largest for blocks with median household income of <$20,000, Black residents, HOLC Grade D, and ungraded industrial areas. UFP concentrations were 4% lower than average for non-Hispanic White residents and higher than average for racialized groups (Asian, 3%; Black, 15%; Hispanic, 6%; Native American, 8%; Pacific Islander, 11%). For blocks with median household incomes of <$20,000, UFP concentrations were 40% higher than average, whereas blocks with incomes of >$110,000 had UFP concentrations 16% lower than average. UFP concentrations were 28% higher for Grade D and 49% higher for ungraded industrial areas compared with Grade A. Disparities were highest for UFPs and lowest for PM2.5 exposure levels. DISCUSSION: Our study is one of the first to highlight large disparities with UFP exposures compared with multiple pollutants. Higher exposures to multiple air pollutants and their cumulative effects disproportionately impact historically marginalized groups. https://doi.org/10.1289/EHP11662.

Ambient Air Pollution Exposure and Sleep Quality in COPD.

Rationale: Ambient air pollution exposure is associated with respiratory morbidity among individuals with chronic obstructive pulmonary disease (COPD), particularly among those with concomitant obesity. Although people with COPD report high incidence of poor sleep quality, no studies have evaluated the association between air pollution exposure, obesity, and sleep disturbances in COPD. Methods: We analyzed data collected from current and former smokers with COPD enrolled in the Subpopulations and Intermediate Outcome Measures in COPD -Air Pollution ancillary study (SPIROMICS AIR). Socio-demographics and anthropometric measurements were collected, and 1-year mean historical ambient particulate matter (PM2.5) and ozone concentrations at participants' residences were estimated by cohort-specific spatiotemporal modeling. Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI), and regression models were constructed to determine the association of 1-year PM2.5 (1Yr-PM2.5) and 1-year ozone (1Yr-ozone) with the PSQI score, and whether obesity modified the association. Results: In 1308 participants (age: 65.8±7.8 years, 42% women), results of regression analyses suggest that each 10µg/m3 increase in 1Yr-PM2.5 was associated with a 2.1-point increase in PSQI (P=0.03). Obesity modified the association between 1Yr-PM2.5 and PSQI (P=0.03). In obese and overweight participants, a 10µg/m3 increase in 1Yr-PM2.5 was associated with a higher PSQI (4.0 points, P<0.01, and 3.4 points, P<0.01, respectively); but no association in lean-normal weight participants (P=0.51). There was no association between 1 Yr-ozone and PSQI. Conclusions: Overweight and obese individuals with COPD appear to be susceptible to the effects of ambient PM2.5 on sleep quality. In COPD, weight and ambient PM2.5 may be modifiable risk factors to improve sleep quality.

Black carbon content in airway macrophages is associated with increased severe exacerbations and worse COPD morbidity in SPIROMICS.

BACKGROUND: Airway macrophages (AM), crucial for the immune response in chronic obstructive pulmonary disease (COPD), are exposed to environmental particulate matter (PM), which they retain in their cytoplasm as black carbon (BC). However, whether AM BC accurately reflects environmental PM2.5 exposure, and can serve as a biomarker of COPD outcomes, is unknown. METHODS: We analyzed induced sputum from participants at 7 of 12 sites SPIROMICS sites for AM BC content, which we related to exposures and to lung function and respiratory outcomes. Models were adjusted for batch (first vs. second), age, race (white vs. non-white), income (<$35,000, $35,000~$74,999, ≥$75,000, decline to answer), BMI, and use of long-acting beta-agonist/long-acting muscarinic antagonists, with sensitivity analysis performed with inclusion of urinary cotinine and lung function as covariates. RESULTS: Of 324 participants, 143 were current smokers and 201 had spirometric-confirmed COPD. Modeled indoor fine (< 2.5 µm in aerodynamic diameter) particulate matter (PM2.5) and urinary cotinine were associated with higher AM BC. Other assessed indoor and ambient pollutant exposures were not associated with higher AM BC. Higher AM BC was associated with worse lung function and odds of severe exacerbation, as well as worse functional status, respiratory symptoms and quality of life. CONCLUSION: Indoor PM2.5 and cigarette smoke exposure may lead to increased AM BC deposition. Black carbon content in AMs is associated with worse COPD morbidity in current and former smokers, which remained after sensitivity analysis adjusting for cigarette smoke burden. Airway macrophage BC, which may alter macrophage function, could serve as a predictor of experiencing worse respiratory symptoms and impaired lung function.

Within-City Variation in Ambient Carbon Monoxide Concentrations: Leveraging Low-Cost Monitors in a Spatiotemporal Modeling Framework.

BACKGROUND: Based on human and animal experimental studies, exposure to ambient carbon monoxide (CO) may be associated with cardiovascular disease outcomes, but epidemiological evidence of this link is limited. The number and distribution of ground-level regulatory agency monitors are insufficient to characterize fine-scale variations in CO concentrations. OBJECTIVES: To develop a daily, high-resolution ambient CO exposure prediction model at the city scale. METHODS: We developed a CO prediction model in Baltimore, Maryland, based on a spatiotemporal statistical algorithm with regulatory agency monitoring data and measurements from calibrated low-cost gas monitors. We also evaluated the contribution of three novel parameters to model performance: high-resolution meteorological data, satellite remote sensing data, and copollutant (PM2.5, NO2, and NOx) concentrations. RESULTS: The CO model had spatial cross-validation (CV) R2 and root-mean-square error (RMSE) of 0.70 and 0.02 parts per million (ppm), respectively; the model had temporal CV R2 and RMSE of 0.61 and 0.04 ppm, respectively. The predictions revealed spatially resolved CO hot spots associated with population, traffic, and other nonroad emission sources (e.g., railroads and airport), as well as sharp concentration decreases within short distances from primary roads. DISCUSSION: The three novel parameters did not substantially improve model performance, suggesting that, on its own, our spatiotemporal modeling framework based on geographic features was reliable and robust. As low-cost air monitors become increasingly available, this approach to CO concentration modeling can be generalized to resource-restricted environments to facilitate comprehensive epidemiological research. https://doi.org/10.1289/EHP10889.

Characterization of Annual Average Traffic-Related Air Pollution Concentrations in the Greater Seattle Area from a Year-Long Mobile Monitoring Campaign.

Growing evidence links traffic-related air pollution (TRAP) to adverse health effects. We designed an innovative and extensive mobile monitoring campaign to characterize TRAP exposure levels for the Adult Changes in Thought (ACT) study, a Seattle-based cohort. The campaign measured particle number concentration (PNC) to capture ultrafine particles (UFP), black carbon (BC), nitrogen dioxide (NO2), fine particulate matter (PM2.5), and carbon dioxide (CO2) at 309 roadside sites within a large, 1200 land km2 (463 mi2) area representative of the cohort. We collected about 29 two-minute measurements at each site during all seasons, days of the week, and most times of the day over a 1-year period. Validation showed good agreement between our BC, NO2, and PM2.5 measurements and monitoring agency sites (R2 = 0.68-0.73). Universal kriging-partial least squares models of annual average pollutant concentrations had cross-validated mean square error-based R2 (and root mean square error) values of 0.77 (1177 pt/cm3) for PNC, 0.60 (102 ng/m3) for BC, 0.77 (1.3 ppb) for NO2, 0.70 (0.3 µg/m3) for PM2.5, and 0.51 (4.2 ppm) for CO2. Overall, we found that the design of this extensive campaign captured the spatial pollutant variations well and these were explained by sensible land use features, including those related to traffic.

Ambient ozone effects on respiratory outcomes among smokers modified by neighborhood poverty: An analysis of SPIROMICS AIR.

BACKGROUND: Neighborhood poverty has been associated with poor health outcomes. Previous studies have also identified adverse respiratory effects of long-term ambient ozone. Factors associated with neighborhood poverty may accentuate the adverse impact of ozone on respiratory health. OBJECTIVES: To evaluate whether neighborhood poverty modifies the association between ambient ozone exposure and respiratory morbidity including symptoms, exacerbation risk, and radiologic parameters, among participants of the SPIROMICS AIR cohort study. METHODS: Spatiotemporal models incorporating cohort-specific monitoring estimated 10-year average outdoor ozone concentrations at participants' homes. Adjusted regression models were used to determine the association of ozone exposure with respiratory outcomes, accounting for demographic factors, education, individual income, body mass index (BMI), and study site. Neighborhood poverty rate was defined by percentage of families living below federal poverty level per census tract. Interaction terms for neighborhood poverty rate with ozone were included in covariate-adjusted models to evaluate for effect modification. RESULTS: 1874 participants were included in the analysis, with mean (± SD) age 64 (± 8.8) years and FEV1 (forced expiratory volume in one second) 74.7% (±25.8) predicted. Participants resided in neighborhoods with mean poverty rate of 9.9% (±10.3) of families below the federal poverty level and mean 10-year ambient ozone concentration of 24.7 (±5.2) ppb. There was an interaction between neighborhood poverty rate and ozone concentration for numerous respiratory outcomes, including COPD Assessment Test score, modified Medical Research Council Dyspnea Scale, six-minute walk test, and odds of COPD exacerbation in the year prior to enrollment, such that adverse effects of ozone were greater among participants in higher poverty neighborhoods. CONCLUSION: Individuals with COPD in high poverty neighborhoods have higher susceptibility to adverse respiratory effects of ambient ozone exposure, after adjusting for individual factors. These findings highlight the interaction between exposures associated with poverty and their effect on respiratory health.

Publicly available low-cost sensor measurements for PM2.5 exposure modeling: Guidance for monitor deployment and data selection.

High-resolution, high-quality exposure modeling is critical for assessing the health effects of ambient PM2.5 in epidemiological studies. Using sparse regulatory PM2.5 measurements as principal model inputs may result in two issues in exposure prediction: (1) they may affect the models' accuracy in predicting PM2.5 spatial distribution; (2) the internal validation based on these measurements may not reliably reflect the model performance at locations of interest (e.g., a cohort's residential locations). In this study, we used the PM2.5 measurements from a publicly available commercial low-cost PM2.5 network, PurpleAir, with an external validation dataset at the residential locations of a representative sample of participants from the Adult Changes in Thought - Air Pollution (ACT-AP) study, to improve the accuracy of exposure prediction at the cohort participant locations. We also proposed a metric based on principal component analysis (PCA) - the PCA distance - to assess the similarity between monitor and cohort locations to guide monitor deployment and data selection. The analysis was based on a spatiotemporal modeling framework with 51 "gold-standard" monitors and 58 PurpleAir monitors for model development, as well as 105 home monitors at the cohort locations for model validation, in the Puget Sound region of Washington State from June 2017 to March 2019. After including calibrated PurpleAir measurements as part of the dependent variable, the external spatiotemporal validation R2 and root-mean-square error, RMSE, for two-week concentration averages improved from 0.84 and 2.22 µg/m3 to 0.92 and 1.63 µg/m3, respectively. The external spatial validation R2 and RMSE for long-term averages over the modeling period improved from 0.72 and 1.01 µg/m3 to 0.79 and 0.88 µg/m3, respectively. The exposure predictions incorporating PurpleAir measurements demonstrated sharper urban-suburban concentration gradients. The PurpleAir monitors with shorter PCA distances improved the model's prediction accuracy more substantially than the monitors with longer PCA distances, supporting the use of this similarity metric.

Deployment, Calibration, and Cross-Validation of Low-Cost Electrochemical Sensors for Carbon Monoxide, Nitrogen Oxides, and Ozone for an Epidemiological Study.

We designed and built a network of monitors for ambient air pollution equipped with low-cost gas sensors to be used to supplement regulatory agency monitoring for exposure assessment within a large epidemiological study. This paper describes the development of a series of hourly and daily field calibration models for Alphasense sensors for carbon monoxide (CO; CO-B4), nitric oxide (NO; NO-B4), nitrogen dioxide (NO2; NO2-B43F), and oxidizing gases (OX-B431)-which refers to ozone (O3) and NO2. The monitor network was deployed in the Puget Sound region of Washington, USA, from May 2017 to March 2019. Monitors were rotated throughout the region, including at two Puget Sound Clean Air Agency monitoring sites for calibration purposes, and over 100 residences, including the homes of epidemiological study participants, with the goal of improving long-term pollutant exposure predictions at participant locations. Calibration models improved when accounting for individual sensor performance, ambient temperature and humidity, and concentrations of co-pollutants as measured by other low-cost sensors in the monitors. Predictions from the final daily models for CO and NO performed the best considering agreement with regulatory monitors in cross-validated root-mean-square error (RMSE) and R2 measures (CO: RMSE = 18 ppb, R2 = 0.97; NO: RMSE = 2 ppb, R2 = 0.97). Performance measures for NO2 and O3 were somewhat lower (NO2: RMSE = 3 ppb, R2 = 0.79; O3: RMSE = 4 ppb, R2 = 0.81). These high levels of calibration performance add confidence that low-cost sensor measurements collected at the homes of epidemiological study participants can be integrated into spatiotemporal models of pollutant concentrations, improving exposure assessment for epidemiological inference.

Racial Segregation and Respiratory Outcomes among Urban Black Residents with and at Risk of Chronic Obstructive Pulmonary Disease.

Rationale: Racial residential segregation has been associated with worse health outcomes, but the link with chronic obstructive pulmonary disease (COPD) morbidity has not been established.Objectives: To investigate whether racial residential segregation is associated with COPD morbidity among urban Black adults with or at risk of COPD.Methods: Racial residential segregation was assessed using isolation index, based on 2010 decennial census and baseline address, for Black former and current smokers in the multicenter SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), a study of adults with or at risk for COPD. We tested the association between isolation index and respiratory symptoms, physiologic outcomes, imaging parameters, and exacerbation risk among urban Black residents, adjusting for established COPD risk factors, including smoking. Additional mediation analyses were conducted for factors that could lie on the pathway between segregation and COPD outcomes, including individual and neighborhood socioeconomic status, comorbidity burden, depression/anxiety, and ambient pollution.Measurements and Main Results: Among 515 Black participants, those residing in segregated neighborhoods (i.e., isolation index ⩾0.6) had worse COPD Assessment Test score (ß = 2.4; 95% confidence interval [CI], 0.7 to 4.0), dyspnea (modified Medical Research Council scale; ß = 0.29; 95% CI, 0.10 to 0.47), quality of life (St. George's Respiratory Questionnaire; ß = 6.1; 95% CI, 2.3 to 9.9), and cough and sputum (ß = 0.8; 95% CI, 0.1 to 1.5); lower FEV1% predicted (ß = -7.3; 95% CI, -10.9 to -3.6); higher rate of any and severe exacerbations; and higher percentage emphysema (ß = 2.3; 95% CI, 0.7 to 3.9) and air trapping (ß = 3.8; 95% CI, 0.6 to 7.1). Adverse associations attenuated with adjustment for potential mediators but remained robust for several outcomes, including dyspnea, FEV1% predicted, percentage emphysema, and air trapping.Conclusions: Racial residential segregation was adversely associated with COPD morbidity among urban Black participants and supports the hypothesis that racial segregation plays a role in explaining health inequities affecting Black communities.

Modeling residential indoor concentrations of PM2.5 , NO2 , NOx , and secondhand smoke in the Subpopulations and Intermediate Outcome Measures in COPD (SPIROMICS) Air study.

Increased outdoor concentrations of fine particulate matter (PM2.5 ) and oxides of nitrogen (NO2 , NOx ) are associated with respiratory and cardiovascular morbidity in adults and children. However, people spend most of their time indoors and this is particularly true for individuals with chronic obstructive pulmonary disease (COPD). Both outdoor and indoor air pollution may accelerate lung function loss in individuals with COPD, but it is not feasible to measure indoor pollutant concentrations in all participants in large cohort studies. We aimed to understand indoor exposures in a cohort of adults (SPIROMICS Air, the SubPopulations and Intermediate Outcome Measures in COPD Study of Air pollution). We developed models for the entire cohort based on monitoring in a subset of homes, to predict mean 2-week-measured concentrations of PM2.5 , NO2 , NOx , and nicotine, using home and behavioral questionnaire responses available in the full cohort. Models incorporating socioeconomic, meteorological, behavioral, and residential information together explained about 60% of the variation in indoor concentration of each pollutant. Cross-validated R2 for best indoor prediction models ranged from 0.43 (NOx ) to 0.51 (NO2 ). Models based on questionnaire responses and estimated outdoor concentrations successfully explained most variation in indoor PM2.5 , NO2 , NOx , and nicotine concentrations.

Contribution of Individual and Neighborhood Factors to Racial Disparities in Respiratory Outcomes.

Rationale: Black adults have worse health outcomes compared with white adults in certain chronic diseases, including chronic obstructive pulmonary disease (COPD).Objectives: To determine to what degree disadvantage by individual and neighborhood socioeconomic status (SES) may contribute to racial disparities in COPD outcomes.Methods: Individual and neighborhood-scale sociodemographic characteristics were determined in 2,649 current or former adult smokers with and without COPD at recruitment into SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). We assessed whether racial differences in symptom, functional, and imaging outcomes (St. George's Respiratory Questionnaire, COPD Assessment Test score, modified Medical Research Council dyspnea scale, 6-minute-walk test distance, and computed tomography [CT] scan metrics) and severe exacerbation risk were explained by individual or neighborhood SES. Using generalized linear mixed model regression, we compared respiratory outcomes by race, adjusting for confounders and individual-level and neighborhood-level descriptors of SES both separately and sequentially.Measurements and Main Results: After adjusting for COPD risk factors, Black participants had significantly worse respiratory symptoms and quality of life (modified Medical Research Council scale, COPD Assessment Test, and St. George's Respiratory Questionnaire), higher risk of severe exacerbations and higher percentage of emphysema, thicker airways (internal perimeter of 10 mm), and more air trapping on CT metrics compared with white participants. In addition, the association between Black race and respiratory outcomes was attenuated but remained statistically significant after adjusting for individual-level SES, which explained up to 12-35% of racial disparities. Further adjustment showed that neighborhood-level SES explained another 26-54% of the racial disparities in respiratory outcomes. Even after accounting for both individual and neighborhood SES factors, Black individuals continued to have increased severe exacerbation risk and persistently worse CT outcomes (emphysema, air trapping, and airway wall thickness).Conclusions: Disadvantages by individual- and neighborhood-level SES each partly explain disparities in respiratory outcomes between Black individuals and white individuals. Strategies to narrow the gap in SES disadvantages may help to reduce race-related health disparities in COPD; however, further work is needed to identify additional risk factors contributing to persistent disparities.

The Association Between Neighborhood Socioeconomic Disadvantage and Chronic Obstructive Pulmonary Disease.

Rationale: Individual socioeconomic status has been shown to influence the outcomes of patients with chronic obstructive pulmonary disease (COPD). However, contextual factors may also play a role. The objective of this study is to evaluate the association between neighborhood socioeconomic disadvantage measured by the area deprivation index (ADI) and COPD-related outcomes. Methods: Residential addresses of SubPopulations and InteRmediate Outcome Measures in COPD Study (SPIROMICS) subjects with COPD (FEV1/FVC <0.70) at baseline were geocoded and linked to their respective ADI national ranking score at the census block group level. The associations between the ADI and COPD-related outcomes were evaluated by examining the contrast between participants living in the most-disadvantaged (top quintile) to the least-disadvantaged (bottom quintile) neighborhood. Regression models included adjustment for individual-level demographics, socioeconomic variables (personal income, education), exposures (smoking status, packs per year, occupational exposures), clinical characteristics (FEV1% predicted, body mass index) and neighborhood rural status. Results: A total of 1800 participants were included in the analysis. Participants residing in the most-disadvantaged neighborhoods had 56% higher rate of COPD exacerbation (P<0.001), 98% higher rate of severe COPD exacerbation (P=0.001), a 1.6 point higher CAT score (P<0.001), 3.1 points higher SGRQ (P<0.001), and 24.6 meters less six-minute walk distance (P=0.008) compared with participants who resided in the least disadvantaged neighborhoods. Conclusion: Participants with COPD who reside in more-disadvantaged neighborhoods had worse COPD outcomes compared to those residing in less-disadvantaged neighborhoods. Neighborhood effects were independent of individual-level socioeconomic factors, suggesting that contextual factors could be used to inform intervention strategies targeting high-risk persons with COPD.